French Maritime Pine Bark Extract Alleviates Lung Injury by Regulating Inflammatory-Oxidative-Apoptotic Pathway and P2X7 Receptor Expression in LPS-Induced Sepsis


ULAŞ N., ÖZKANLAR S., YILDIRIM S., AYDIN Ö., Özkanlar Y.

CURRENT ISSUES IN MOLECULAR BIOLOGY, cilt.47, sa.9, 2025 (SCI-Expanded, Scopus)

  • Yayın Türü: Makale / Tam Makale
  • Cilt numarası: 47 Sayı: 9
  • Basım Tarihi: 2025
  • Doi Numarası: 10.3390/cimb47090770
  • Dergi Adı: CURRENT ISSUES IN MOLECULAR BIOLOGY
  • Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus, EMBASE, Directory of Open Access Journals
  • Ondokuz Mayıs Üniversitesi Adresli: Hayır

Özet

Introduction: Sepsis is a dysregulated systemic immune response to infection which may result in mortality. It may also lead to organ injury, including injury to the lung. French maritime pine bark extract (MPBE) has been proposed to prevent/treat various inflammatory diseases due to its strong anti-inflammatory and antioxidant effects. This study evaluates the protective and therapeutic effects of MPBE on lung injury induced by intraperitoneal E. coli lipopolysaccharide (LPS) in rats. Materials and Methods: The study design was as follows: Control, MPBE20, MPBE50, LPS, LPS+MPBE20 and LPS+MPBE50. Blood and lung tissue samples were collected 6 h after the LPS induction following a 10-day administration of MPBE. Results: LPS-induced sepsis was confirmed by the overproduction of IL-1 beta and TNF-alpha in bloodstream compared to the Control (p < 0.001). Lung injury was determined by severe histopathological changes and neutrophil infiltration in the lung tissue following intraperitoneal LPS injection. In lung tissue, MPBE improved the levels of P2X7R, TLR4, NLRP3, IL-1 beta, TNF-alpha, JNK, H2AX, 8-OHdG, MDA, GSH, Caspase-1 and Caspase-3, and pathological changes in MPBE+LPS groups compared to the LPS group. Conclusions: MPBE appears to regulate P2X7R signaling and the inflammatory-apoptotic pathway by protecting the lung from oxidative cell damage in LPS-induced sepsis in vivo.